Respiratory Flashcards

1
Q

4 most common drugs against TB

A

(Isoniazid) INH: primary drug used
rifampin
ethambutol
pyrazinamide

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2
Q

Isoniazid MOA

A

Suppresses bacterial growth by inhibiting synthesis of mycolic acid, a component of the mycobacterial cell wall.
Metabolized in the liver through acetylation—watch for “slow acetylators”

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3
Q

Isoniazid A/E and what to administer in high risk pt groups

A

Hepatotoxicity
Peripheral neuropathy
- Administer pyridoxine (Vitamin B6) daily in high risk groups (i.e., DM, ETOH abuse) or if patient develops neuropathy

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4
Q

Rifampin MOA

A

MOA: inhibits bacterial DNA-dependent RNA polymerase -> results in suppression of RN synthesis and protein synthesis

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5
Q

A/E of Rifampin

A

discoloration of bodily fluids

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6
Q

2 Analogs of Rifampin (close chemical make-up with same MOA and A/E)

A

Rifapentine

Rifabutin

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7
Q

Pyrazinamide (PZA) A/E

A

Non-gouty polyarthralgias – (pain in multiple joints)

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8
Q

Ethanbutol A/E

A

Optic neuritis – blurred vision, constriction of visual fields, & disturbance of color discrimination (red-green color blindness).

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9
Q

What is the most effective drug class for prevention / treatment of seasonal & perennial rhinitis - it reduces inflammation and edema

A

Intranasal Glucocorticoids (-sone)

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10
Q

Difference between H1 and H2 blockers (antihistamine)

A

H1 blockers are the drugs to which most people are referring when they use the term antihistamine. H1 blockers prevent the harmful effects of histamine and are used to treat seasonal allergic rhinitis, anaphylaxis, reactions to insect bites, and so forth.
H2 blockers are used to treat gastric acid disorders

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11
Q

When to take first generation antihistamines?

A

take at bedtime to avoid sedation

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12
Q

How to recognize first generation anti-histamine?

A

-amine

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13
Q

Common second generation anti-histamines?

A

Zyrtec, Claritin, Clarinex, Allegra

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14
Q

What is major difference between first and second generation anti-histamines?

A

Second generation poorly cross the blood-brain barrier; have a low affinity for H1 receptors in the CNS therefore does not cause sedation

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15
Q

Sympathomimetics (Decongestants) MOA

A

Reduce nasal congestion via activation of alpha1 adrenergic receptors on nasal blood vessels -> vasoconstriction

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16
Q

A/E to decongestants?

A
Rebound congestion (topicals) used for more than 5 days
CNS stimulation (oral) – restlessness, anxiety, insomnia
CV effects (oral) – tachycardia, inc. BP
17
Q

Three classes of bronchodilators

A

beta2-adrenergic agonists
anticholinergics
xanthine derivatives

18
Q

Give two categories of beta2 agonists and common drugs in each

A

Short Acting Beta Agonists: Albuterol
(think -buterol) Levalbuterol
Pirbuterol
Metaproterenol
Long acting beta agonist: Arformoterol
(think -moterol) Formoterol
Salmeterol

19
Q

LABA are not used alone in management of asthma. What additional class is added to regime?

A

Inhaled Corticosteroids (-sone or -sonide)

20
Q

Anticholinergics MOA

A

Acetylcholine (ACh) causes bronchial constriction and narrowing of the airways.
Anticholinergics bind to the ACh receptors, preventing ACh from binding.
Result: bronchoconstriction is prevented, airways dilate

21
Q

Xanthines MOA

A

Action: inhibits phophodiesterase, an enzyme responsible for breaking down cAMP. Because this enzyme is inhibited, more cAMP is available for bronchodilation.

22
Q

Common Xanthine drugs (THEO-DUR)

A

Theophylline / iv form - aminophylline

23
Q

First and late sign of toxicity in patients receiving xanthine drug

A

Early - Nausea

Late - Tremors, Dysrhythmia and Convulsions

24
Q

Leukotriene Receptor Antagonist MOA

A

Leukotrienes are substances released when a trigger, such as cat hair or dust, starts a series of chemical reactions in the body.
Leukotrienes cause inflammation, bronchoconstriction, and mucus production
By blocking those receptors, you block that cascade

25
Leukotriene receptor antagonist suffix
-kast
26
Mast Cell Stabilizers MOA
Stabilize mast cells, reducing the release of mast cell chemicals that cause bronchoconstriction, edema, and inflammation. Interrupts migration of eosinophils into site
27
Common Mast Cell Stabilizer drug
Cromolyn
28
Inhaled Corticosteroids (ICS) MOA
Work by suppressing inflammation Decrease synthesis & release of inflammatory mediators including leukotrienes, histamine, prostaglandins Decrease infiltration & activity of inflammatory cells including eosinophils, leukocytes Decrease edema of the airway mucosa 2nd to a decrease in vascular permeability
29
A/E of the -sone or -sonide drugs (ICS)
Oropharyngeal candidiasis | Dysphonia (hoarseness)
30
Step-wise approach to asthma control
Step 1 Short-acting inhaled beta2 agonist as needed Step 2 Preferred: low-dose inhaled corticosteroid (ICS). -Alternative: cromolyn, nedocromil, leukotriene receptor antagonist (LTRA), or theophylline Step 3 Low-dose ICS and long-acting beta2 agonist (LABA) or medium-dose ICS -Alternative: low-dose ICS and either LTRA, theophylline, or zileuton Step 4 Preferred: medium-dose ICS plus LABA -Alternative: medium-dose ICS plus either LTRA, theophylline, or zileuton Step 5 High-dose ICS and LABA, and consider omalizumab for patients with allergies Step 6 High-dose ICS and LABA and oral corticosteroid, and consider omalizumab for patients with allergies
31
Anticholinergic Agents (how to recognize) and contraindicated in which patient population
-tropium bromide / may increase intraocular pressure - glaucoma pt's
32
Expectorants MOA and common drug
``` remove viscid (sticky) secretions by reduction of the adhesiveness & surface tension. Guaifenesin (aka musinex and robitussin) ```
33
Antitussive MOA
Suppresses the cough reflex in the medulla
34
Common opioid antitussive | Common non-opioid antitusive
Codeine | Dextromethorphan and Benzonatate
35
Acetylcysteine is common drug found in which class; MOA
Mucolytic Agents; Action – works directly on mucus to reduce thickness & make secretions less tenacious.
36
What drug is indicated for patient with acetaminophen overdose?
Acetylcysteine
37
Pulmonary arterial hypertension pathophysiology
Pulmonary hypertension is a type of high blood pressure that affects the arteries in the lungs and the right side of the heart. Pulmonary hypertension begins when tiny arteries in lungs, called pulmonary arteries, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through the lungs, and raises pressure within the lungs' arteries. As the pressure builds, your heart's lower right chamber (right ventricle) must work harder to pump blood through your lungs, eventually causing your heart muscle to weaken and eventually fail.
38
3 drug classes indicated for pulmonary hypertension
Prostacyclin Analogs Endothelian 1 receptor antagonist Phosphodiesterase Type 5 Inhibitors (-afil)
39
Lung surfactant: Porcine extract of lung surfactant given to neonates w/ respiratory distress syndrome (how to recognize drug)
-actant